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The purpose of this review is to integrate recent research on the respiratory immune effects of e-cigarettes with the pathogenesis of asthma to better understand how e-cigarettes may affect asthmatics and to note critical knowledge gaps regarding the effects of e-cigarettes on asthmatics.

Human, rodent, and cell culture studies show that key cellular functions of epithelial cells, macrophages, and neutrophils are altered by e-cigarette exposure. Because respiratory immunity is already dysregulated in asthma, further alteration of cellular function by e-cigarettes could impact asthma development, severity, and/or exacerbations. Future research is needed to more directly investigate this relationship using controlled human exposure studies and exposure of cell culture or animal models of asthma to e-cigarettes.

Human, rodent, and cell culture studies show that key cellular functions of epithelial cells, macrophages, and neutrophils are altered by e-cigarette exposure. Because respiratory immunity is already dysregulated in asthma, further alteration of cellular function by e-cigarettes could impact asthma development, severity, and/or exacerbations. Future research is needed to more directly investigate this relationship using controlled human exposure studies and exposure of cell culture or animal models of asthma to e-cigarettes.There is a lack of class I evidence concerning the impact of surgery in the treatment of diffuse low-grade glioma; the early maximal resection with preservation of eloquent brain areas has been accepted as the first therapeutic option. We performed a systematic review of the literature using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and protocol. Selleck KU-57788 Inclusion criteria only case series with at least 100 patients containing supratentorial hemispheric diffuse low-grade glioma (according to any of the WHO classification used in papers published between 2000 to 2019), with pre- and postoperative MRI study were included in the qualitative and quantitative analyses. The extent of resection should be defined based on MRI at least in two categories and correlated with patients’ outcomes (with univariate or multivariate analyses) using overall survival (OS) or malignant progression-free survival (MPFS). A total of 18 series with 4386 patients, published in 20 papers, were included in this systematic review. All the series that evaluates the relation between the extent of resection (EOR) and OS showed a statistically significant improvement of OS at univariate and/or multivariate analyzes with a greater EOR. Six studies showed a statistically significant improvement of MPFS with a greater EOR. We demonstrate that when a more rigorous analysis of EOR is performed, a benefit of a more aggressive resection on OS and MPFS is observed. Our review about EOR in different molecular groups of DLGG also suggests a benefit of maximum safe resection for all different subtypes, even though “radical surgery” may be associated with better OS and MPFS in tumors with a more aggressive signature.Concussion is a widely recognized environmental risk factor for neurodegenerative diseases, including Parkinson’s disease (PD). Small-vessel disease of the brain has been reported to contribute to neurodegenerative diseases. In this study, we observed BBB disruption in wild-type (WT) mice, but not in matrix metalloproteinase 9 (MMP-9) knockout mice, subjected to single severe traumatic brain injury (ssTBI). Furthermore, treating ssTBI mice with the MMP-9 inhibitor GM6001 effectively maintained BBB integrity, promoted the elimination of damaged mitochondria via mitophagy, and then prevented neuronal death and progressive neurodegeneration. However, we did not observe this neuroprotective effect of MMP-9 inhibition in beclin-1-/+ mice. Collectively, these findings revealed that concussion led to BBB disruption via MMP-9, and that GM6001 prevented the development of PD via the autophagy pathway.

Circulating tumor cells (CTCs) have been shown to be heterogeneous. Focusing on the epithelial-mesenchymal transition and perioperative kinetics, we evaluated CTCs with mesenchymal phenotypes as a potential prognostic biomarker for patients with gastric cancer.

Peripheral blood was collected from 54 patients with gastric cancer before surgery and at 1week and 1month after surgery. CTCs were enriched using density-gradient centrifugation and magnetic-activated cell sorting (negative selection). Cell suspensions were characterized by multi-immunofluorescence staining against cytokeratin and N-cadherin, and by 4′,6′-diamidino-2-phenyldole staining.

CTCs were detected in five patients (17%) with early cancer and 14 patients (56%) with advanced cancer (p < 0.05). In our system, N-cadherin, but not cytokeratin, was expressed in the CTCs of 90% (19/21) of patients. Postoperative recurrence was detected in 10 patients, all of whom had N-cadherin+/cytokeratin-/CD45- CTCs preoperatively. Regarding perioperative kinetics, we divided patients into three risk groups a high-risk group, with one or more preoperative CTCs and increased CTCs postoperatively; an intermediate-risk group, with one or more preoperative CTCs and decreased CTCs postoperatively; and a low-risk group, with no preoperative CTCs. Recurrence rates were 57% (4/7), 33% (4/12), and 6% (2/35), respectively. The relapse-free survival rate was lower in patients at high risk versus those at intermediate or low risk, for all patients (p = 0.00024) and in patients with advanced cancer (p = 0.00103).

N-cadherin is a highly useful marker to detect CTCs lacking cytokeratin, and the perioperative kinetics of CTC numbers is beneficial in risk stratification for survival in patients with gastric cancer.

N-cadherin is a highly useful marker to detect CTCs lacking cytokeratin, and the perioperative kinetics of CTC numbers is beneficial in risk stratification for survival in patients with gastric cancer.This study probes the function and mechanism of lymphocyte-specific protein 1 (LSP1) in glioblastoma pathogenesis. According to the data acquired from TCGA, Oncomine and GEO databases, the expression and prognostic value of LSP1 and miR-920 in glioblastoma patients were analyzed. The expression levels of LSP1 in U251 and A172 cell lines were analyzed by qRT-PCR and western blotting. CCK8, colony formation and transwell assays were utilized to test glioblastoma cell malignant abilities. Furthermore, the associations between LSP1 and miR-920 were indentified by bioinformatics analysis and rescue assays. Moreover, the protein expression levels of p-JAK2, JAK2, p-STAT5 and STAT5, as the hallmark of JAK/STAT5 signaling, were detected by western blotting. The observations showed that LSP1 was highly augmented in glioblastoma samples. Additionally, up-regulation of LSP1 was associated with a unfavorable prognosis in glioblastoma patients. Biological experiments revealed that depletion of LSP1 significantly suppressed the proliferation, invasion and migration of U251 and A172 cells.